Group .beta.-hemolytic Streptococcus (GBS) are ubiquitous microorganisms. GBS is not known to cause any harmful infections in humans except for very young babies. GBS pneumonia, also called "early-onset disease", is associated with high morbidity and mortality in newborn infants. The GBS infection may be present on the day of birth and is particularly frequent in premature babies. After the infants reach a few weeks of age and normal lung development has occurred, they are no longer subject to GBS pneumonia.
In a series of studies conducted by Dr. Carl G. Hellerqvist and his associates at the Vanderbilt University School of Medicine, Nashville, Tennessee, a polysaccharide GBS toxin was identified. This toxin, which is elaborated by Group B .beta.-hemolytic Streptococcus is believed to be a major factor in the complications of GBS pneumonia.
The GBS toxin has been isolated from GBS culture media, purified, and partially characterized. See Hellerqvist, et al. (1981), Pediatr.Res., 15:892-898; Rojas, et al. (1981), Pediatr.Res., 15:899-904; Rojas, et al. (1983), Pediatr. Res., 17:1002-1008; and Hellerqvist, et al. (1987), Proc. Natl. Acad. Sci. USA, 84:51-55. In these studies, sheep were used as an experimental model for testing the effect of the GBS polysaccharide toxin on lungs. Differing from human, the lungs of mature sheep as well as young sheep are subject to GBS toxin. When the toxin is infused into sheep it produces pulmonary hypertension and increased pulmonary vascular permeability. These changes are similar to those occurring in newborn infants with Group B streptococcal sepsis.
GBS toxin is a complex polysaccharide with an estimated molecular weight of around 200,000. This polysaccharide shares immunological structural features with the group antigen as reported in Hellerqvist et al. (1981), cited above, and contains phosphodiester structures deemed essential directly or indirectly to toxin function [Hellerqvist, et al. (1987), cited above.]